N-Acetyl Cysteine is a widely available nutritional supplement, one of my favorites. It is used medically to treat Tylenol poisoning. It is an excellent anti-oxidant, and is particularly effective at scavenging aldehydes, like acetaldehyde from alcohol. It increases levels of glutatione, one of the bodies primary anti-oxidants.

This increase in glutathione increases neurotransmitter binding ability, thus improving the effectiveness of existing neurotransmitters like serotonin, dopamine, norepinephrine. It has been shown to be highly effective in Parkinson's disease, a dopamine deficiency state. Again, it doesn't increase dopamine per se, it improves receptor sensitivity.

Now, there is another reason to take it as evidenced by the below studies.

Several lines of evidence suggest that oxidative stress may play a role in the behavioral changes and neurotoxicity in rats after administration of methamphetamine (MAP). N-acetyl-l-cysteine (NAC) is a precursor of glutathione, and it also exerts as an antioxidant. In this study, we investigated the effects of NAC on the behavioral changes (hyperlocomotion and development of sensitization) and neurotoxicity in male Wistar rats after administration of MAP. Pretreatment with NAC (30, 100 or 300 mg/kg, i.p.) attenuated significantly hyperlocomotion in rats induced by a single administration of MAP (2 mg/kg, i.p.), in a dose-dependent manner. Furthermore, pretreatment with NAC (100 mg/kg, i.p., 15 min before MAP injection, once daily for 5 consecutive days) blocked significantly the development of behavioral sensitization in rats after repeated administration of MAP (2 mg/kg, once daily for 5 consecutive days), whereas the behaviors in rats after repeated administration of NAC plus saline groups were not different from those of control (vehicle plus saline) groups. One week after administration of MAP (7.5 mg/kgx4, 2-h intervals), levels of dopamine (DA) in rat striatum were significantly decreased as compared with control groups. Pretreatment with NAC (1, 3, 10 or 30 mg/kg, i.p., 30 min before each MAP injection) attenuated significantly the MAP-induced reduction of DA in rat striatum, in a dose-dependent manner. These results suggest that NAC could prevent the behavioral changes (acute hyperlocomotion and development of behavioral sensitization) in rats and neurotoxicity in rat striatum after administration of MAP, and that NAC would be a useful drug for treatment of several symptoms associated with MAP abuse.

1Department of Psychiatry, Chiba University Graduate School of Medicine, Chiba, Japan.

Several lines of evidence suggest that oxidative stress might contribute to neurotoxicity in the dopaminergic nerve terminals after administration of methamphetamine (MAP). We undertook the present study to determine whether intravenous administration of N-acetyl-L-cysteine (NAC), a potent antioxidant drug, could attenuate the reduction of dopamine transporter (DAT) in the striatum of monkey brain after administration of MAP. Positron emission tomography studies demonstrated that repeated administration of MAP (2 mg/kg as a salt, four times at 2-h intervals) significantly decreased the accumulation of radioactivity in the striatum after intravenous administration of [(11)C]beta-CFT. In contrast, the binding of [(11)C]SCH 23390 to dopamine D(1) receptors in the monkey striatum was not altered after the administration of MAP. A bolus injection of NAC (150 mg/kg, i.v.) 30 min before MAP administration and a subsequent continuous infusion of NAC (12 mg/kg/h, i.v.) over 8.5 h significantly attenuated the reduction of DAT in the monkey striatum 3 weeks after the administration of MAP. These results suggest that NAC could attenuate the reduction of DAT in the monkey striatum after repeated administration of MAP. Therefore, it is likely that NAC would be a suitable drug for treatment of neurotoxicity in dopaminergic nerve terminals related to chronic use of MAP in humans.Neuropsychopharmacology advance online publication, 16 June 2004; doi:10.1038/sj.npp.1300512

PMID: 15199373 </DD>

jaimegerise

07-06-04, 05:16 PM

Reminder, please post medication information in the Meds section of the forums. Thread was originally posted in ADDults section.

:D

FlakeyGirl

07-06-04, 05:32 PM

Very interesting. Could you elaborate a little on how this supplement helps you, I mean in a practical non-theoretical way. Do you know off hand if there are any drug interaction concerns? Also, if I am taking NAC every morning, will tylenol work if I get a fever in the afternoon. I wonder if the action would differ between i.v. administration and ingestion (assuming thats how the nutritional supplements are taken)? .....always curious about something that could help out my poor little dopamine receptors.

lynx

07-06-04, 06:35 PM

The only caution with NAC is that some people recommend 3x as much vitamin C should be taken with it in order to keep it in its reduced form, however, in the studies they used NAC alone.

Personally I take vitamin C anyway, just for general health. And it won't prevent your tylenol from working, however,if you want to protect you dopamine receptors never take tylenol, it massively depletes glutathione. That is its primary mode of toxicity, glutathione depeletion. Glutathione depletion will leave your brain vulnerable to all sorts of insults, in fact people that take tylenol over prolonged periods have a higher risk of Alzheimer's. Take motrin, it protects your brain against aging/decline.

Good luck

FlakeyGirl

07-06-04, 07:58 PM

I can't really take ibubrofen, I have a vascular condition that prevents it.

Other than antioxidant properties, I am still not quite understanding how NAC benefits you, personally. And in what way if any does digestion affect NAC?